Downregulated placental expression of linc00468 contributes to trophoblast dysfunction by inducing epithelial-mesenchymal transition

Downregulated placental expression of linc00468 contributes to trophoblast dysfunction by inducing epithelial-mesenchymal transition
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linc00468 胎盘表达下调通过诱导上皮间质转化导致滋养层功能障碍

DOI:
10.21037/atm.2020.02.166
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发表时间:
2020-03
影响因子:
--
通讯作者:
Sun Lizhou
Sun Lizhou
中科院分区:
医学4区
文献类型:
--
作者:
Wang Sailan;Wu Dan;Xu Yetao;Cao Yueying;Wang Jiawei;Zhang Yuanyuan;Yang Nana;Sun Lizhou

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Background Preeclampsia (PE) is a widespread progressive condition that can occur pregnancy and is related to high maternal morbidity and fetal mortality in the perinatal period. However, the exact mechanism responsible has not been specific. Accumulating evidence has highlighted the prominent role of the epithelial‐mesenchymal transition (EMT) in the biological behaviors of PE. Methods We explored the role of a lincRNA in extravillous trophoblast (EVTs) cell viability, migration, invasion and apoptosis in vitro, along with the use of linc00468 knockdown or overexpression. Clinically, we discovered that the expression of linc00468 was frequently correlated with adverse clinical features and poor prognosis of PE patients. Results We uncovered that linc00468 was downregulated in PE samples compared to in healthy tissues and in trophoblast cells. Functionally, gain and loss-of-function experiments demonstrated that linc00468 inhibited cell proliferation, migration, invasion and linc00468 accelerated apoptosis of the trophoblast phenotype in cell lines. Moreover, we demonstrated that downregulation of linc00468 promoted the expression of E-cadherin and β-catenin but reduced the expression of N-cadherin, Vimentin and Snail, resulting in progression of EMT. Conclusions In conclusion, linc00468 promoted EMT and a consequent increase in invasiveness in HTR-8/Svneo and JAR EVT cell lines. Our study provides the first evidence that linc00468 has a pivotal role in cell invasion and promotes intrinsic and extrinsic EMT ability of PE.
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